"We have evaluated a number of compounds that influence the growth of lung cancer cells. We have reported previously on the autocrine role of gastrin releasing peptide, insulin-like growth factor, and transferrin. These factors stimulate growth for certain types of lung cancers. We have also shown that regulatory molecules such as glucagon and 13-cis-retinoic acid can inhibit the growth of a number of lung cancer cell lines. This experience has allowed us to focus on signal transduction pathways that are central to regulating cancer cell growth and potentially amenable to clinical intervention. We have published data suggesting that 5-HETE, a product of 5-lipoxygenase activation, may be a key intermediary in growth factor mediated growth stimulation of cancer cells. We have shown that lung cancer cells frequently express the message for 5-lipoxygenase. These cells also express an associated molecule critically required for lipoxygenase-mediated growth effects (five lipoxygenase activating protein, FLAP). Using selective lipoxygenase inhibitors that have been developed for other medical applications, reduced the growth of tumor cells. We have demonstrated with an in vivo model that this anti-proliferative effect of blocking the lipoxygenase pathway is potentially mediated via an apoptotic mechanism. We now also have data suggesting that the same approach that we reported for lung cancer is equally relevant to breast cancer and prostate cancer . This is important mechanistic information could allow rapid translation into clinical prevention application. Several lipoxygenase inhibitors could be evaluated in Phase I/II prevention trials and we are comparing the in vivo characteristics to decide the best candidate to take to clinical evaluation."